Sandrina Körner

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Four-day cyclic rats fed 7, 12-dimethylbenz(a)anthracene (dmba) (20 mg) at 50 days of age had peak prolactin, oestradiol and uterine wet weights at pro-oestrus. Tamoxifen (50, 200 and 800 mug daily), administered to ovariectomized rats, produced significant (P less than 0 X 05) decreases in oestrogen-stimulated prolactin levels but was unable to reduce(More)
Macrophage-dependent antitumoral activity is partly mediated by soluble factors including cytokines, reactive-oxygen intermediates (ROIs), and reactive-nitrogen intermediates (RNIs). Activation of macrophages for tumor cytotoxicity can be achieved with various bacterial compounds, such as lipopolysaccharides (LPSs), muramyl-dipeptides, and lipopeptides. We(More)
Aqueous extracts (ENOCW) and enzymatic digests of purified Nocardia opaca cell wall fragments, virtually free of muramyl peptides, were monitored for their phagocytic response modifying reactivity on polymorphonuclear leucocytes, separated or unseparated in whole human blood. In the presence of ENOCW a 74% increased production of superoxide during the(More)
  • Dlamini N, Voermans Nc, +108 authors Jungbluth H Recessive
  • 2013
Clinical and neuropathological features of X-linked spinal muscular atrophy (SMAX2) associated with a novel mutation in the UBA1 gene. (NEB) mutations in a childhood onset distal myopathy with rods and cores uncovered by next generation sequencing. might be the first manifestation of a genetic disorder. Novel deletion of lysine 7 expands the clinical,(More)
A major molecular pathway of genetic instability in cancer is DNA mismatch repair deficiency, leading to accumulation of numerous mutations at repetitive DNA sequence stretches (microsatellites), known as high-level microsatellite instability (MSI-H). In colorectal cancer, MSI-H tumors show a clinical behavior different from microsatellite-stable (MSS)(More)
Antibody-dependent cellular cytotoxicity (ADCC) of natural killer (NK) cells largely contributes to the success of monoclonal antibody (mAb) treatment in cancer. As no antibodies are clinically available for immunotherapy of myeloid leukemias (MLs), we aimed to develop an Fc-optimized CD133 mAb for induction of NK ADCC against MLs. When comparing different(More)
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